In the majority of this predominantly non-Hispanic white referred sample of obese children, overweight started in the preschool years. The referral to the endocrinologist, occurring after a prolonged interval from the obesity onset, was ineffective in treating obesity. Hyperinsulinemia and hypercholesterolemia are often present also at a young age. These obesity comorbidities in association with high prevalence of parental obesity and type 2 diabetes expose these youths to high risk for developing type 2 diabetes and coronary heart disease. Our data underscore the need for early family-based behavioral-lifestyle intervention programs to be made available to pediatricians, enabling them to target the "at risk for overweight" preschool children and their likely overweight parents.

To evaluate the contemporary prevalence of diabetic peripheral neuropathy (DPN) in participants with type 1 diabetes in the T1D Exchange Clinic Registry throughout the U.S. RESEARCH DESIGN AND METHODSDPN was assessed with the Michigan Neuropathy Screening Instrument Questionnaire (MNSIQ) in adults with ‡5 years of type 1 diabetes duration. A score of ‡4 defined DPN. Associations of demographic, clinical, and laboratory factors with DPN were assessed. RESULTSAmong 5,936 T1D Exchange participants (mean 6 SD age 39 6 18 years, median type 1 diabetes duration 18 years [interquartile range 11, 31], 55% female, 88% non-Hispanic white, mean glycated hemoglobin [HbA 1c ] 8.1 6 1.6% [65.3 6 17.5 mmol/mol]), DPN prevalence was 11%. Compared with those without DPN, DPN participants were older, had higher HbA 1c , had longer duration of diabetes, were more likely to be female, and were less likely to have a college education and private insurance (all P < 0.001). DPN participants also were more likely to have cardiovascular disease (CVD) (P < 0.001), worse CVD risk factors of smoking (P 5 0.008), hypertriglyceridemia (P 5 0.002), higher BMI (P 5 0.009), retinopathy (P 5 0.004), reduced estimated glomerular filtration rate (P 5 0.02), and Charcot neuroarthropathy (P 5 0.002). There were no differences in insulin pump or continuous glucose monitor use, although DPN participants were more likely to have had severe hypoglycemia (P 5 0.04) and/or diabetic ketoacidosis (P < 0.001) in the past 3 months. CONCLUSIONSThe prevalence of DPN in this national cohort with type 1 diabetes is lower than in prior published reports but is reflective of current clinical care practices. These data also highlight that nonglycemic risk factors, such as CVD risk factors, severe hypoglycemia, diabetic ketoacidosis, and lower socioeconomic status, may also play a role in DPN development.Diabetic neuropathy is a prevalent complication in patients with diabetes and a major cause of morbidity and mortality (1). Among the various forms of diabetic neuropathy, distal symmetric polyneuropathy (DPN) and diabetic autonomic neuropathies are by far the most studied (1).

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We measured adult heights (Ht) of 94 healthy GH-sufficient children (peak GH > 10 ng/mL, polyclonal RIA) whose Ht at presentation were more than 2 SD below the mean for chronological age, with normal weight-to-Ht ratios, normal body proportions, and pathologic growth velocity for chronological age. Group 1 (n 36, 6 females) received standardized doses (0.3 mg/kg x week) of GH (mean duration = 41 months), while group 2 (n = 58, 17 females) received no treatment. Our conclusion was that the mean final Ht SD score in the GH-treated group (-1.5) was significantly greater than in the untreated group (-2.1); P < .001. Genetic predisposition to short stature was evident in both groups: the midparental Ht SD score was -1.1 in the treated and -1.0 in the untreated group. Midparental Ht was met or exceeded by 42% of the GH-treated group but only 15% of the untreated group. Final Ht was not significantly different from predicted Ht, except from GH-treated girls, who exceeded their predicted Ht. Although the mean Ht gains (6.8 cm in girls and 3 cm in boys) were modest and variable, GH treatment provided significantly better Ht outcomes for the majority of children with idiopathic growth failure.

Birth length has been reported to be either normal or reduced in infants with congenital GH deficiency (CGHD). We evaluated 46 infants with CGHD followed in a single regional medical center. All were born full term and had peak GH of less than 10 microg/liter after provocative stimulation. Length SD score at birth was normal but subsequently showed deceleration, at 6 months and 12 months of age, before GH treatment. The majority were delivered vaginally (83%), and delivery was uncomplicated in 61%. Four patients (9%) had breech vaginal delivery. Perinatal morbidities were found in 72% of infants and included jaundice (n = 17), hypoglycemia with or without seizure (n = 14), and hypoxemia (n = 5). Multiple pituitary hormone deficiencies were found in 85% of the subjects. Organic lesions were documented in all 22 subjects who had magnetic resonance imaging and in 4 of 11 subjects who had computed tomography scan. Only the hypoglycemic infants received early GH treatment. Growth data in hypoglycemic and normoglycemic CGHD infants were not significantly different. In our population, CGHD did not adversely affect fetal growth but is essential for normal linear growth during early infancy. Congenital developmental abnormalities in the hypothalamic-pituitary region are the most common cause of CGHD and are best diagnosed by an magnetic resonance imaging study.